Endocrine changes associated with a rapidly developing sodium appetite in rats.
Endocrine changes associated with a rapidly developing sodium appetite in rats.
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DOI：
10.1152/ajpregu.1994.267.5.r1168
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发表时间：
1994-11
期刊：
影响因子：
--
通讯作者：
R. Thunhorst;M. Morris;A. K. Johnson
中科院分区：
文献类型：
--
作者：
R. Thunhorst;M. Morris;A. K. Johnson
同时给予利尿剂呋塞米（10 mg/kg）和低剂量的血管紧张素转换酶（ACE）抑制剂卡托普利（5 mg/kg）导致短潜伏期口渴和钠食欲（即，快速摄入水和NaCl溶液）。为了阐明介导该行为的潜在机制，在接受该处理方案的大鼠中表征了参与液体摄入和平衡的关键激素的血浆水平的变化。与单独使用任一药物治疗的大鼠相比，联合使用呋塞米和低剂量卡托普利治疗的大鼠血浆肾素活性和血管紧张素I增加，但血浆醛固酮增加相当。呋塞米加低剂量卡托普利治疗增加血浆加压素，但不增加血浆催产素。较高剂量的卡托普利（100 mg/kg）与呋塞米（一种不刺激液体摄入的药物组合）联合给药（29），进一步增加了血浆肾素活性和血管紧张素I，但阻止了血浆加压素的升高。结果支持这一假设，即口渴和盐的食欲产生的协议依赖于血管紧张素II形成的脑室周器官，而不是体循环。
Simultaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg) results in short-latency thirst and sodium appetite (i.e., the rapid ingestion of water and NaCl solution). To elucidate potential mechanisms for mediating this behavior, changes in plasma levels of key hormones involved in fluid intake and balance were characterized in rats subjected to this treatment protocol. Rats treated jointly with furosemide and low-dose captopril had exaggerated increases in plasma renin activity and angiotensin I but equivalent increases in plasma aldosterone compared with rats treated with either agent alone. Treatment with furosemide plus low-dose captopril increased plasma vasopressin but not plasma oxytocin. The administration of a higher dose of captopril (100 mg/kg) with furosemide, a combination of drugs that does not stimulate fluid intake (29), further increased plasma renin activity and angiotensin I but prevented the rise in plasma vasopressin. The results support the hypothesis that thirst and salt appetite generated by this protocol depend on angiotensin II formed within brain circumventricular organs rather than the systemic circulation.